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Pretreatment with β-glucan attenuates isoprenaline-induced myocardial injury in rats
1Department of Physiology, Faculty of Veterinary Medicine, University of Erciyes, 38039, Kayseri, Turkey.
New Findings:
What is the central question of this study? The study was designed to assess whether pretreatment with β-glucan could exert any protective action against isoprenaline-induced myocardial injury in rats. What is the main finding and its importance? β-Glucan pretreatment could reduce myocardial injury by restoring cardiac biomarkers, antioxidant status, apoptosis and histopathological changes. Therefore, β-glucan might have the potential to be used in the prevention and/or treatment of myocardial infarction.
Abstract:
This study was designed to investigate the cardioprotective effect of pretreatment with β-glucan, the glucose polymer derived from the yeast Saccharomyces cerevisiae, against isoprenaline (ISO)-induced myocardial injury in rats by studying biochemical cardiac markers, antioxidant parameters, apoptosis, ECG and histopathological changes. Male Sprague-Dawley rats were randomly divided into four treatment groups, namely control, β-glucan, isoprenaline and β-glucan + isoprenaline. The β-glucan treatment group received β-glucan (50 mg kg-1 day-1 , p.o.) for 10 days. Myocardial injury was induced by ISO administration (100 mg kg-1 , s.c.) twice, at an interval of 24 h, on the 9th and 10th days. Isoprenaline administration resulted in a marked increase in heart rate, ST segment elevation, myocardial malondialdehyde content, cardiac marker levels (lactate dehydrogenase, creatine kinase-MB and high-sensitivity cardiac troponin T) and apoptotic index, and a significant decrease in R-wave amplitude and myocardial superoxide dismutase, catalase and glutathione peroxidase activities. In addition, apoptosis, congestion, necrosis, inflammatory cell infiltration and myofibrillar disorganization were observed histologically in myocardial tissue sections. The oral pretreatment with β-glucan prevented almost all the parameters of isoprenaline-induced myocardial injury in rats, and these findings were confirmed by the histopathological analysis. These findings provide evidence that β-glucan could protect rat myocardium against ISO-induced myocardial injury, and this was attributed to its antioxidant and anti-apoptotic properties.
Insights
Beta-glucan pretreatment demonstrated protective effects against heart damage in rats. It improved cardiac biomarkers, antioxidant status, and reduced cell death, suggesting potential for myocardial infarction prevention and treatment.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Biochemistry
Background:
- Myocardial infarction remains a leading cause of mortality worldwide.
- Isoprenaline (ISO) is commonly used to induce myocardial injury in animal models.
- Exploring natural compounds for cardioprotection is an active area of research.
Purpose of the Study:
- To evaluate the cardioprotective potential of beta-glucan against ISO-induced myocardial injury in rats.
- To investigate the effects of beta-glucan on cardiac biomarkers, oxidative stress, and apoptosis.
Main Methods:
- Male Sprague-Dawley rats were pretreated with beta-glucan (50 mg/kg/day, p.o.) for 10 days.
- Myocardial injury was induced by subcutaneous administration of isoprenaline (100 mg/kg).
- Cardiac markers, antioxidant enzyme activities, apoptosis, ECG, and histopathology were assessed.
Main Results:
- Isoprenaline significantly increased cardiac markers, oxidative stress, and apoptosis, while decreasing antioxidant levels.
- Beta-glucan pretreatment attenuated ISO-induced increases in cardiac markers and oxidative stress.
- Beta-glucan reduced the apoptotic index and prevented histopathological damage in rat myocardium.
Conclusions:
- Beta-glucan exhibits significant cardioprotective effects against isoprenaline-induced myocardial injury in rats.
- The protective mechanisms involve antioxidant and anti-apoptotic properties.
- Beta-glucan holds promise as a therapeutic agent for preventing or treating myocardial infarction.
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